I have argued that the evolutionary raison d'etre of beta 2-microglobulin H-2 or HLA antigens dimmers has always been to serve as the plasma membrane anchorage site of organogenesis-directing antigens, such as testis-organizing H-Y, during development. Accordingly, competitive displacements of these functionally important host antigens with their own became an integral part of the viral strategy, and that observed H-2 or HLA restrictions in T-cell killings of virally infected or transformed target cells are merely the inevitable evolutionary consequence of the above. Our preliminary studies indicated that on the plasma membrane of pure testicular Sertoli cells, B- as well as T-cells of the H-2 compatible females recognize the identical set of two antigens; testis-organizing H-Y and a cell-type specific antigen that Sertoli cells share with ovarian follicular cells. T-cell killings of Sertoli cells were H-2 restricted, if directed against the former, but unrestricted if directed aganist the latter antigen. We would like to expand on the above study also using other cell types, such as testicular Leydig cells, as the targets. If it is proven that H-2 restrictions occur only with regard to organogenesis-directing plasma membrane antigens, we shall gain a considerable insight into the nature of the viral strategy noted above. The use of testicular Sertoli or Leydig cells as the targets brings about an additional benefit. As they are so much larger than attacking T-cells, one can actually observe and cinematographically record the actual killing by educated T-cells of target cells under a microscope. We wish to study the kinetics of T-cell killings using unprimed T-cells as the control.